The protein kinase C activator, phorbol ester, elicits disparate functional responses in androgen-sensitive and androgen-independent human prostatic cancer cells
The protein kinase C activator, phorbol ester, elicits disparate functional responses in androgen-sensitive and androgen-independent human prostatic cancer cells
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DOI：
10.1006/bbrc.1998.8238
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发表时间：
1998-03-06
影响因子：
3.1
通讯作者：
Vihko, P
中科院分区：
文献类型：
--
作者：
Henttu, P;Vihko, P
蛋白激酶C （PKC）激活剂12- o -十四烷醇-磷酸-13-乙酸酯（TPA）在雄激素敏感的LNCaP细胞中激活细胞死亡，而在雄激素非依赖性的DU-145或PC-3细胞中没有激活细胞死亡，PKC抑制剂staurosporine和H7显著降低了这些细胞的生长。所有细胞系的PKC总活性水平相似，但其对Ca2+离子和脂质的依赖性不同，受TPA的调节也不同。此外，TPA仅在LNCaP和DU-145细胞中上调了直接早期基因c-fos和c-jun的表达，而PC-3细胞未表达c-fos mRNA。在LNCaP细胞中，TPA对c-myc mRNA的调控与细胞死亡激活呈负相关，在雄激素非依赖性细胞系中略有升高。这些结果表明PKC信号转导通路在雄激素敏感和不敏感的前列腺细胞中具有不同的功能。(C) 1998学术出版社。
The protein kinase C (PKC) activator 12-O-tetradecanoyl-phorbol-13-acetate (TPA) activated cell death in androgen-sensitive LNCaP cells but not in androgen-independent DU-145 or PC-3 cells, whose growth was significantly decreased by PKC inhibitors staurosporine and H7. All cell lines had similar levels of total PKC activities which, however, differed on their dependency on Ca2+ ions and lipid and were regulated differently by TPA. Furthermore, expression of the immediate early genes c-fos and c-jun was up-regulated by TPA only in LNCaP and DU-145 cells, whereas PC-3 cells failed to express c-fos mRNA. The regulation of the c-myc mRNA by TPA correlated inversely with activation of cell death being down-regulated in LNCaP cells, and slightly increased in the androgen-independent cell lines. These results suggest that the PKC signal transduction pathway functions differently in androgen-sensitive and insensitive prostatic cells. (C) 1998 Academic Press.